Conductive hearing loss (CHL)-such as is caused by middle ear infections and other ear conditions-can affect the auditory system in a profound and detrimental manner. The disruptions caused by CHL are often impairments of binaural hearing tasks that require the integration of information from both ears, such as the filtering of sounds in noisy and reverberant environments. Long-term speech and language impairments can result from CHL. Still today, the exact manner in which long-term CHL affects the central auditory system is not entirely known, but it is clear that the effects can be severe and long lasting. The cluster of symptoms that result are termed Central Auditory Processing Disorder (or (C)APD). Currently, diagnosis of (C)APD is difficult, requiring a battery of tests and months of time. This s problematic, since studies have shown that it is beneficial to treat (C)APD as early as possible. One potential metric that could be used to assess binaural hearing function and diagnose (C)APD is the binaural interaction component (BIC) of the auditory brainstem response (ABR). The sound-evoked binaural interaction component (BIC) is the residual auditory brainstem response (ABR) remaining after subtracting the binaurally evoked ABR from the sum of the monaurally evoked ABRs. The peak is the first negative peak in the BIC, which is related to binaural processing. Latencies of in both human and animal studies indicate it has a brainstem origin at the level of the inferior colliculus and its inputs. The inferior colliculus isa site of convergence of inputs from all brainstem nuclei, including nuclei of the superior olivary complex, which computes binaural acoustical cues to location (interaural time (ITD) and level (ILD) differences). The BIC may have important diagnostic value; for example, altered latencies and amplitudes of the peak in children and adults are correlated with and predictive of the same long-term behavioral deficits in binaural processing associated with chronic CHL. In this proposal, we investigate the effect of CHL on the BIC peak and correlate the BIC with a behavioral measure of sound localization ability, the acoustic startle response. The amplitude of and latency of the BIC peak will be assessed across a range of ITD and ILD cues to location during the course of an induced unilateral CHL, and sound localization behavior will be assessed at corresponding time points. We hypothesize that CHL alters the integration of sound localization cues in a predictable way, which will enhance our understanding of the effect of CHL on binaural hearing. Furthermore, we expect that both behavior and BIC will recover with time, with BIC predicting the level of sound localization ability. Understanding the interaction between sound localization and the BIC promises to yield a clinically useful tool for assessing binaural hearing ability and CHL in children with otitis media. This proposal is specifically designed to provide training in both basic science and clinical aspects of auditory research, furthering the mission of the NIDCD.